Thank you all for coming, you know it's a it's really I'm hoping you're all learning a lot and please give us feedback as to you know what we can do for the future and to let us know what worked and what didn't here. So hard to know everyone has a different background so I'm gonna just try to give a general overview of what we do when we have a patient with ventricular tachycardia come into the lab. These are my disclosures, I do not receive any personal honorarium from from the companies. So this is a case a typical 63 year old gentleman with coronary disease had an old large anterolateral infarction in 2010 and has a big apical aneurysm, a set up to have arrhythmias in that particular case, has a cardiomyopathy and had an ICD implanted initially for primary prevention, has had you know heart failure but really very mild, has a low ejection fraction, 55% being normal, his is 20 but it's not really been in the hospital for heart failure. This time or came in last year with sustained monomorphic ventricular tachycardia and this just happened to be slow enough below the rate of where the defibrillator was set. Since he had never had the arrhythmia before we didn't know how fast the arrhythmia would be but this was pretty slow actually just 400 milliseconds which is about a hundred and fifty beats a minute. The device was reprogrammed in the emergency room and he was started on amiodarone. However he started to have frequent ICD shocks for ventricular tachycardia despite getting additional amiodarone and occasionally when it would try to pace him out of it it would degenerate into a very rapid rhythm called polymorphic VT after attempted therapy so he got a lot of shocks. So he had a catheterization which showed that that left anterior descending artery was totally occluded. That was an old problem. He had collaterals from the right to the left and he has no angina, no chest pain symptoms. His labs are normal and this is what his EKG showed. I apologize for the quality but it was a tracing initially from another hospital. All right well anyway you could see in V1 it's a left bundle kind of appearance and it's a negative in the inferior lead so coming in the lower part of the heart and going up and probably somewhere on the septum. This is what the EKG, they cardioverted him in the ER initially and this is what it looked like after converting to sinus arrhythmia. He has this old heart attack, the anterior wall MI, Q waves out to that area and this is really pretty much the same as his old EKG. Hasn't changed and no evidence for having an acute MI. So I gotta just ask for a show of hands. I know you're not gonna know really the answer to this but do you want to do like something to fix his artery? He has that old blockage in the artery. You either can do something acutely you know with at the time of the catheterization you could do a PCI or a stent. Do you want to do bypass surgery? Do you want to add another drug to the amiodarone or would you ablate him? Anyone do either one or two? Hard to say right? Adding another drug or what do you think about the last answer? Anyone want to just ablate him? I think that's everyone wants to do that. Okay and that's what we wanted to do also because this is the perfect kind of scenario to really you know reduce morbidity. I'll have him you know not get shocked all the time and you know hopefully not have him on long-term amiodarone if we can avoid the long-term toxic effects of that drug. So this is what we do in the lab. We could see that you know in the lab he actually was having so much of this and it almost seemed like he was having more and more as time went on. He has this is the EKG similar to his 12 lead. The leads may be on a little differently but it's the same tachycardia arrived in the lab with and we can look at the defibrillator and we can actually take those electrograms and compare them to what he's having whatever we induce in the lab and we could say is this the tachycardia is having all the time and then what other tachycardia is he has besides that and this is the one that we were able to induce even when he wasn't in it and this is all the same by looking at the appearance of that signal in the right ventricle from the defibrillator. And then we do a voltage map. So this particular technology is electro-anatomic mapping where we can actually see what the signal amplitude looks like in sinus rhythm. So where's the scar and no surprise it's where he had his heart attack right so he has anterolateral MI he's got a big scar all that red means scar that's the low voltage 0.04 1.5 as normal as the purple and everything else is in between. We call that the border zone in between the really scarred area and the normal myocardium. So we can localize where this is and coming from and usually the arrhythmia comes from the area of that border zone frequently and then we have areas that even when we paste or we couldn't see any signals but even when we paste we couldn't paste we call that electrically unexcitable. And then you know it's someone who doesn't tolerate their arrhythmia a good way is to kind of look and do a little pace mapping and pacing in different areas and trying to find what looks like that ventricular tachycardia is this one and none of these are really even close to perfect but these two might be a little better than some of the others in this region here looks a little bit when we take our catheter and we pace looks very similar or more similar to his tachycardia but the problem in this case usually we could do this more more and more sites but he kept going into the arrhythmia it was just incessant. So we were actually fortunate in the lab he was tolerating it very well so our classic way of doing before we had all these fancy you know mapping systems we we had to just you know use what we what we could and we used to use what was called entrainment mapping we still do if they can tolerate this well enough we can during the arrhythmia we can pace from the ablation catheter that's right in the area where we think it might be coming from so we have a general vicinity of where we know it's coming from and we pace in those areas to try to reproduce the way that QRS complex looks on the EKG with our pace complex and so and then when he's in ventricular tachycardia we can do this entrainment and there's certain criteria we utilize to say are we in the scar we in the isthmus where we are in those areas so and then we can so that's what we're doing here and you can see when we're pacing it looks identical to his tachycardia and so that might be a good site and there's some other things we look for to determine if it is or isn't and then we also look on our ablation catheter which is this one down here it looks like it might not be too prominent for some reason my oops yeah sorry about that somehow it's not going back but let's try that again here we go so this signal here is that what we call the diastolic potential and sometimes we can see that in an area of an important area of the scar in what's called you know the isthmus and this is where our is if you were using fluoroscopy we use less and less fluoroscopy but you could see the catheter that's at the tip of the let me see if I could even use a pointer might be easier this doesn't work either but so here this catheter here is the ablation catheter and it's here at the tip and that was where the the some of the better pace maps were and then we deliver the energy this was radiofrequency energy and you can see that the arrhythmia is is actually right we just started in this area but it was slowed down and it terminated but we know we're not done because this scar is big and you know you want to try to you know you'll give more lesions and this is what we wound up doing and we look for things we look for the best pace maps and then we also look for these little you know fragmented potentials and and that might indicate scar and then after that we couldn't get that tachycardia but we got a lot other we got other ones and this was we were lucky only two other ones were induced in the EP lab and they were successfully ablated too so you want to as much as the patient's tolerating it want to ablate everything you possibly can at the first sitting but sometimes you you know you can't you could only do so much depending on how well they're tolerating it and then usually what we'll do before they go home is to get them get them off the drug if you can the amiodarone in this case and then to do a non-invasive stimulation through the defibrillator to see if we get any more ventricular tachycardia and we only got with very closely coupled stimuli a very polymorphic non-clinical arrhythmia so we thought that was a good sign and he went home and so it's eight months or more now he hasn't had any arrhythmias now we do have some guidelines I'm going to briefly mention but we have some guidelines of when we should send people for ablation now this was your classic case that he had multiple episodes of ventricular tachycardia or VT storm we call it and he was not really I'm you know I wasn't working anyway and it's a high level of recommendation we call that a class one recommendation and the other point and you all didn't pick this and fall into that trap but if you revascularize someone so you think well that LAD was a problem that anterior descending artery if I fix that will he do better that doesn't do anything this is an old infarct this area of scar there's a fixed substrate that's not going to do you any good and so most people that we know now we have these these this great technology that even if they don't tolerate their arrhythmia and it's not mappable with all that entrainment mapping we have this technology that can identify scar and identify these areas of the border zone in the area where the tachycardia may be coming from and pretty much you know most or most at least a third or more patients have both of this easy tolerated mappable VT as well as unmappable VT and so that the the concept again being that reentry is the underlying mechanism and most of these patients who have ischemic heart disease and that dense scar is here the border zone is the rainbow in here and then and that's where most of the arrhythmias arise and then here's the normal myocardium and we use you know we look for these channels of where things may be coming from we do this pace and pacing during arrhythmia to look for where that isthmus is so we might be able to treat and ablate and you know in other patients we may not they may be really compromised hemodynamically and unstable or you might have multiple VTs so so we want to have some other mechanisms to map and so it's really turned things around having all this technology available and it's better for the patient because we can map in sinus rhythm and this is just showing you an example of mapping that's a really good match I didn't have one earlier but for this particular case you could see on the left is his arrhythmia on the right is where we're pacing and there are a really good match because that area is close to where the arrhythmia is exiting and then we look for these things I we look for these potentials and they you might think it's just a little noise but where those arrows are pointing here you could see this diastolic or this late potential an area of abnormal conduction sometimes we get really fragmented electrograms that look like that and you know sometimes we just see these isolated potentials and we can you change our equipment look for where these channels might be we can try to localize that better and then so what's the success rate so this is just a one summary paper Bill Stevenson's lab put this together as a summary of if you use all these tech all this technology how often can you create you know make them non-inducible after doing this you know and do a good job acutely well pretty well I mean we do pretty well they still have a defibrillator as backup and VT can recur though it's we don't tell them it's a cure either from that site but even more commonly from another site of the scar so in summary it's the substrate mapping concept is useful in characterizing this anatomic substrate for patients we can actually ablate in areas based on those kind of criteria I showed you pace mapping you could do entrainment if you can but looking for late potentials and you know these channels we think it's safer so we don't have to keep the patient in the arrhythmia very long but we use it in conjunction with our life-saving therapy defibrillators

ventricular tachycardia

lab

treatment

electro-anatomic mapping

ablation therapy